Neuroscience is the scientific study of the nervous system. The principle mechanism underlying enhanced pain sensitivity is a persistent hyperexcitability of spinal dorsal horn neurons. This book describes cellular mechanisms for the maintained hyperexcitability of spinal dorsal horn neurons mediated by neuron-glia interactions following spinal cord injury. In addition, nerve growth factor (NGF) has a key role not only in the development of sensory and autonomic neurons, but also in the processes of nociception. This book examines the recent evidence of the involvement of NGF in painful diseases and suggests the potential usefulness of anti-NGF strategies as novel analgesics for disabling pathological conditions. Furthermore, neuralgia is a symptom of some neurological disorders and can be found at any age. The pain that accompanies it is usually brief but may be severe. The authors present evidence sustaining the hypothesis that neuralgia (understood as being a shooting/shock-like paroxysmal pain) is a clinical expression of a transcriptional channelopathy. Other chapters in this book review the underlying mechanisms and the anatomical loci/shared circuits between epilepsy and memory, along with the relationship of various neurotransmitters involved. The morphological and functional characteristics of hereditary choroidal dystrophies are also examined, as well as the potential implications of neuroplasticity in dorsal vagal complex (DVC) in the adaptation of gastrointestinal functions.
Author(s): Andres Costa, Eugenio Villalba
Series: Horizons in Neuroscience Research
Publisher: Nova Science Pub Inc
Year: 2010
Language: English
Pages: 452
Tags: Биологические дисциплины;Физиология животных;Нейрофизиология животных;
HORIZONS IN NEUROSCIENCE RESEARCH, VOLUME 1......Page 3
CONTENTS......Page 7
PREFACE......Page 9
SUMMARY......Page 19
ABBREVIATIONS......Page 21
INTRODUCTION......Page 23
1.1. The Characteristics of Nerve Growth Factor......Page 24
1.2.1. Tyrosin Kinase (TrkA) Receptor......Page 25
1.2.2. P75ntr Receptor......Page 26
1.3.1. Tyrosine Kinase Receptor A Signaling......Page 27
1.3.2. Cell Signaling Via P75ntr Receptor......Page 29
1.3.3.1. Transactivation Between the Tyrosine Kinase A and Adrenergic Receptors......Page 32
1.3.3.2. Transactivation Between the TrkA and Adenosine A2 Receptors......Page 34
REFERENCES......Page 35
2.1. Neuronal Tissues......Page 39
2.2. Nonneuronal Tissues......Page 40
2.2.1. Bone Marrow......Page 42
2.2.2. Lung Tissues......Page 43
2.2.3. Adipose Tissues......Page 44
2.2.5.1. Adrenal Glands......Page 45
2.2.5.2Pituitary Gland......Page 46
2.2.5.3.Thyroid Glands......Page 47
REFERENCES......Page 48
3.1. Nerve Growth Factor Modulates the Inflammatory Responses Via Prostaglandins......Page 52
3.1.1. Nerve Growth Factor Associates with the Inflammatory Pain......Page 54
3.2.1. Characterization of the Allergic Responses......Page 55
3.2.3. Nerve Growth Factor is Involved in the Allergic Inflammation Associated with Fibrosis......Page 58
3.3. Relationship Between Nerve Growth Factor and Apoptosis......Page 60
3.4.1. Suppressor Regulatory T Cells in the Autoimmune Diseases......Page 65
3.4.2. Neurogenic Inflammation......Page 68
3.4.2.1. Nerve Growth Factor Regulatory Role in the Autoimmune Diseases......Page 69
3.5.1. Stress Induced Endocrine Alterations......Page 71
3.5.2. The Relationship Between the Stress Induced Endocrine and Cytokine Processes......Page 74
3.5.3. Nerve Growth Factor During Stress Links to the Endocrine and Immune Networks......Page 76
3.5.4. The Network Between the Stress Induced Inflammation and the Actions of the Nerve Growth Factor. The Neurogenic Pain......Page 78
3.6.1 The Effects of Stress, Glucocorticoids, Norepinephrines and CRH on the Direction Towards Th2 Dominance......Page 80
3.6.2 The Immunocompetent Cells Express Glucocorticoid and Catecholamine Receptors......Page 81
3.6.4 Cytokines Promote the Th2 Dominance......Page 82
REFERENCES......Page 83
4.1. The Enhanced Sympathoadrenal Activity and the Modulatory Effects of Catecholamines on the Nerve Growth Factor......Page 93
4.2.1. Catecholamines-Induced Cardiac Hypertrophy......Page 95
4.2.2.1. Phosphatidylinositol 3-Kinase (PI-3K) in the Myogenesis......Page 96
4.2.2.2. Skeletal Muscle Hypertrophy......Page 97
REFERENCES......Page 98
5.1. Nerve Growth Factor in Wound Healing......Page 101
5.2. Nerve Growth Factor Therapy......Page 102
REFERENCES......Page 103
6.1.1. Autoimmune Processes in Graves’ Ophthalmopathy......Page 104
6.1.2. Enhanced Sympathoadrenal Activity in the Thyroid, Adipose and Eye Muscle Tissue Hypertrophy......Page 105
6.2.1. Regulation of the Sympathoadrenal System and the Hypothalamic-Pituitary-Adrenal Axis in Diabetes Mellitus......Page 107
6.2.2. Diabetic Neuropathy and Nerve Growth Factor......Page 108
6.2.3. The Role of Cellular Integrity and Function in Diabetic Vascular Complications......Page 109
REFERENCES......Page 111
ABSTRACT......Page 115
INTRODUCTION......Page 116
INTRACELLULAR MECHANISMS OF NGF ACTION......Page 117
PATHOPHYSIOLOGICAL MECHANISMS OF INFLAMMATORY AND NEUROPATHIC PAIN......Page 119
EXPERIMENTAL EVIDENCE FOR THE INVOLVEMENT OF NGF IN INFLAMMATORY AND NEUROPATHIC PAIN......Page 121
PATHOPHYSIOLOGICAL MECHANISMS OF MIGRAINE......Page 127
PATHOPHYSIOLOGY OF FIBROMYALGIA......Page 128
INVOLVEMENT OF NGF IN THE PATHOPHYSIOLOGICAL MECHANISMS OF MIGRAINE AND FIBROMYALGIA......Page 129
POTENTIAL OF NGF TARGETING STRATEGIES IN NEUROPATHIC PAIN, CHRONIC MIGRAINE AND FIBROMYALGIA......Page 133
CONCLUSIONS......Page 136
REFERENCES......Page 137
ABSTRACT......Page 151
1. INTRODUCTION......Page 152
2.1.1. Chronic fatigue syndrome and autonomic imbalance......Page 154
2.1.2. Psychometric assessment of fatigue in CFS and relation with autonomic imbalance......Page 155
2.2.1. Overtraining syndrome and autonomic imbalance......Page 156
2.2.2. Mood alterations and relation with autonomic imbalance......Page 157
Stage 2: Overreaching / Fatigue......Page 159
Stage 3: Overtraining / Chronic fatigue......Page 160
3.1. HRV as a method of assessing postprandial sympathovagal balance......Page 161
3.2. Prandial pattern and the problem of meal definition......Page 162
3.3.2. Cephalic phase of insulin release......Page 163
3.4. Lipoprivic feeding......Page 164
3.6. Portal glucose receptors, vagal afferents and eating behavior......Page 165
REFERENCES......Page 167
ABSTRACT......Page 179
INTRODUCTION......Page 180
THE MAIN PLAYERS IN THE SIGNAL CASCADE OF ACTIN REMODELING......Page 182
FROM CHROMATIN REMODELING TO NEUROGENESIS......Page 183
REGULATION OF GENE ACTIVITY AT POSTTRANSLATION LEVEL......Page 184
CHROMATIN STRUCTURE: STUDIES IN DROSOPHILA......Page 186
SECOND LEVEL OF GENOME ORGANIZATION: STRUCTURAL ORGANIZATION OF A CHROMOSOME, EUCHROMATIC AND HETEROCHROMATIC REGIONS OF THE DROSOPHILA POLYTENE CHROMOSOMES......Page 190
GENE SILENCING......Page 191
THIRD LEVEL O GENOME ORGANIZATION: SPATIAL ORGANIZATION OF CHROMOSOMES IN THE NUCLEUS......Page 195
EPIGENETIC MECHANISMS IN MEMORY FORMATION......Page 200
CONCLUSION......Page 202
REFERENCES......Page 204
“GLIOPATHY” MAINTAINS PERSISTENT HYPEREXCITABILITY OF SPINAL DORSAL HORN NEURONS AFTER SPINAL CORD INJURY: SUBSTRATE OF CENTRAL NEUROPATHIC PAIN......Page 213
ASCENDING PAIN PATHWAY......Page 214
HYPEREXCITABILITY OF SPINAL DORSAL HORN NEURONS......Page 215
P38 MAPK......Page 217
pERK......Page 218
pCREB......Page 219
PHENOTYPES OF SPINAL DORSAL HORN NEURONS......Page 221
Glial Activation Following Spinal Cord Injury......Page 223
Neuronal-Glial Interactions......Page 225
Loss of Endogenous GABAergic Inhibitory Tone......Page 226
Modulation of Endogenous Inhibitory Circuits: Glial Modulation of GABAergic Tone......Page 228
Loss of Endogenous Opioidergic Inhibitory Tone......Page 230
Modulation of Endogenous Inhibitory Circuits : Glial Modulation of Opioid Effects......Page 231
CONCLUSION......Page 232
REFERENCES......Page 233
ABSTRACT......Page 243
INTRODUCTION......Page 244
1. 1. Diversity of Nicotinic Receptors in the Cns......Page 245
1. 2. Complex Regulation of the Nachrs......Page 247
1. 3. Complexity of the Nicotinergic System as a Neurotransmitter System......Page 249
2. EFFECTS OF ACTIVATING NACHRS......Page 253
2.1. Nicotine-Induced Dehydrogenase Activation......Page 254
2.2. Nicotine -Induced Increases in Nerve Growth Factor......Page 257
2.3. Nicotine -Induced Increase in Cyclooxygenase-2......Page 259
3. CONCLUSION......Page 263
REFERENCES......Page 264
ABSTRACT......Page 275
1. BASIC OF CALCIUM SIGNALING......Page 276
1.1 Calcium Release from Intracellular Calcium Stores......Page 277
1.2 Calcium Influx from Extracellular Source......Page 278
1.3 Capacitative Calcium Entry......Page 279
1.4 Recovery Following Calcium Signaling......Page 280
2. INTRACELLULAR CALCIUM SIGNALING......Page 281
2.1 Neurotransmitter-Mediated [Ca2+]I Response......Page 282
2.2 Inflammatory Molecule-Evoked [Ca2+]I Response......Page 283
2.3 Bioactive Lipid-Evoked [Ca2+]I Response......Page 285
3. INTERCELLULAR CALCIUM SIGNALING......Page 286
4.1 Calcium Signaling and Information Processing in the Enteric Nervous System......Page 287
4.2 Calcium Signaling and Cellular Functions in Enteric Glial Cells......Page 288
REFERENCES......Page 289
ABSTRACT......Page 291
INTRODUCTION......Page 292
CLASSICAL CONDITIONING......Page 293
Cocaine and Attention in Humans......Page 296
Locus of Action for Cocaine and its Implications for Learning......Page 297
Cocaine and Classical Conditioning......Page 298
Evidence from other Drugs Related to Cocaine......Page 299
CONCLUSION......Page 300
REFERENCES......Page 301
ABSTRACT......Page 307
THE DISEASE PROCESS......Page 308
TREATMENT......Page 310
a) Synaptic plasticity/Long term potentiation/ Excitatory amino acids:......Page 313
c) GABA......Page 314
d) Shared circuits by epilepsy and memory:......Page 315
CONCLUSION......Page 316
REFERENCES......Page 317
ABSTRACT......Page 323
BLOOD SUPPLY TO THE LUMBAR NERVE ROOT......Page 324
FEMORAL NERVE STRETCH TEST (FNST) AND STRAIGHT LEG RAISING (SLR) TEST......Page 325
Intraoperative FNST......Page 326
Intraoperative SLR Test......Page 327
Nerve Root Movement During FNST and SLR Test......Page 328
CHANGES OF INTRARADICULAR BLOOD FLOW (IRBF) INDUCED BY INTRAOPERATIVE FNST AND SLR TEST......Page 330
Intraoperative FNST......Page 331
Report of a Case......Page 332
NERVE ROOT PRESSURE DURING NERVE STRETCH TEST......Page 333
PATHOPHYSIOLOGY OF NERVE ROOT COMPRESSION DURING NERVE STRETCH TEST......Page 334
REFERENCES......Page 336
INTRODUCTION......Page 341
Inheritance and Pathology......Page 342
Electrophysiological Alterations......Page 343
Ophthalmoscopic Alterations......Page 344
III.1. Central Areolar Choroidal Dystrophy......Page 345
Ophthalmoscopic Alterations......Page 346
Inheritance......Page 347
Differential Diagnosis......Page 348
Symptoms......Page 349
Ophthalmoscopic Alterations......Page 350
Electrophysiology......Page 352
Electrophysiological Differential Diagnosis......Page 353
REFERENCES......Page 354
ABSTRACT......Page 359
2. BRAINSTEM VAGAL CIRCUITS......Page 360
3.2 Physiological Adaptation......Page 361
4.1 Changes in Physiological States......Page 363
4.2 Alterations During Pathological Conditions......Page 364
5.1 Presence of Neural Stem Cells in Adult DVC......Page 365
5.3 Neural Proliferation in Vivo......Page 367
5.5 Regulation of Neurogenesis......Page 368
REFERENCES......Page 370
ABSTRACT......Page 373
INTRODUCTION......Page 374
RESULTS AND DISCUSSION......Page 376
CONCLUSION......Page 380
REFERENCES......Page 381
INTRODUCTION......Page 385
AMINO ACID-SENSING IN THE INTESTINE......Page 386
CCK and 5-HT......Page 387
AMINO ACID-SENSING IN THE PORTAL VEIN AND LIVER......Page 388
MUCOSAL MECHANISM OF THE GUT AMINO ACID SENSING BY THE ABDOMINAL VAGUS......Page 389
PHYSIOLOGICAL SIGNIFICANCE OF THE LUMINAL AMINO ACID SENSING IN THE BODY NUTRITION HOMEOSTASIS......Page 391
REFERENCES......Page 392
1.1 Schizophrenia......Page 397
1.2 Proteomics and Biomarkers......Page 398
2.1 Dysfunction of Energy Metabolism......Page 399
2.2 The Role of the Oligodendrocytes......Page 400
2.4 Involvement of Immune System......Page 401
2.6 Newly Described Proteins in Schizophrenia and Proteins with Unknown Function......Page 402
3. CONCLUSIONS......Page 403
REFERENCES......Page 404
ABSTRACT......Page 409
REFERENCES......Page 412
INDEX......Page 415
